Copper and iron are essential elements that play critical roles in several biological processes, including cancer cell survival and metabolism. Their dysregulation can cause cellular stress and malfunction, ultimately leading to regulated cell death (RCD). Recently, cuproptosis and ferroptosis have emerged as newly discovered RCDs, reflecting promising results in the context of cancer management. Unlike other RCDs, ferroptosis and cuproptosis have distinct morphological, genetic, and biological mechanisms. Accumulated iron-driven ferroptosis and copper-induced cuproptosis disturb several cellular processes by altering key proteins, signalling pathways, and cell cycles. These disruptions ultimately lead to mitochondrial dysfunction, formation of excessive reactive oxygen species (ROS), impairment of lipid layers, and modulation of immunological functions, altogether paving the direction towards cancer suppression and providing novel avenues towards targeted therapeutic strategies. Therefore, this study aimed to understand the fundamental mechanisms of ferroptosis and cuproptosis, especially in cancer cell mortality. Furthermore, this study highlights the multifaceted roles of phytocompounds, nanomedicines, and chemotherapeutic agents in inducing ferroptosis and cuproptosis. Thus, contributing to significant improvements in the development of cancer treatments.

Among the most significant risks that many chemotherapeutic drugs currently encounter is the development of multidrug resistance (MDR) in cancerous cells. Numerous critical regulators are thought to be responsible for MDR and render therapeutic strategies inefficient. Several pathways mediate this effect, one of which is the upregulation of ATP-binding cassette (ABC) superfamily membrane transporters. Most of these transporters, which regarded as drug efflux pumps, are embedded in the cell membrane and include MDR-associated protein 1 (MRP1/ABCC1), MRP2, P-glycoprotein (MDR1/ABCB or P-gp), and breast cancer resistance protein (BCRP/ABCG2). The exploration of new potential modulators to diminish tumor MDR through natural product-derived compounds has emerged as a prominent research domain worldwide. Among different plant-derived natural compounds, terpenoids have recently attracted attention owing to their extensive health advantages. Multiple preclinical findings have primarily explored plant-derived terpenoids for their MDR-modulatory activities. Plant-based terpenoids counteract MDR by modulating signaling pathways or expression of pertinent proteins or genes. Thus, this review summarizes preclinical experimental data to elucidate the functional roles of terpenoids in MDR reversal by targeting ABC transporters and sheds light on future research on terpenoid-based cancer therapy.

Declining soil fertility and extensive use of chemical fertilizers threaten the long-term sustainability of cereal production in semiarid regions of India.

Parthenium hysterophorus, identified as Congress weed, presents a considerable risk to agricultural ecosystems and human health owing to its invasive characteristics and allelopathic properties. In this study, we explore the potential of biosynthesized silver nanoparticles (AgNPs) using actinobacteria as a sustainable and effective product for inhibiting the growth of P. hysterophorus. Actinobacteria, known for their diverse metabolic capabilities, were isolated and utilized for the eco-friendly synthesis of AgNPs. The reaction mixture consisted of an aqueous silver nitrate solution (1 mM) and the cell-free culture supernatant of Actinobacteria, which served as a source of reducing and stabilizing metabolites for the biosynthesis of silver nanoparticles. The resultant AgNPs were characterised employing several analytical techniques, such as UV-Vis spectroscopy and transmission electron microscopy. The synthesized AgNPs exhibited distinct physicochemical properties such as a surface plasmon resonance peak at ~ 420 nm, spherical shape, nanoscale size of 20.2 nm, confirming their successful formation. Subsequently, the inhibitory activity of actinobacteria-synthesized AgNPs against P. hysterophorus was evaluated through comprehensive bioassays. The nanoparticles demonstrated remarkable inhibition of seed germination, seedling growth, and overall plant development. Moreover, the AgNPs displayed selective toxicity towards Parthenium weed while maintaining minimal impact on non-target plants, emphasizing their potential as a targeted and environmentally friendly solution. The study highlights the promising role of actinobacteria-synthesized AgNPs in managing P. hysterophorus, providing valuable insights into the development of sustainable strategies for weed control. This research contributes to the growing field of nanobiotechnology, showcasing the potential of bioengineered nanoparticles as an effective means to address invasive plant species and promote sustainable agricultural practices.

Pancreatic cancer remains a formidable global health challenge, ranking as the twelfth most common malignancy yet claiming an outsized toll with dismal 5-year survival rates 13.3%, largely due to late-stage diagnosis and limited therapeutic options. This comprehensive review delves into the transformative potential of peptides as innovative biomarkers and prognostic indicators, addressing the critical gaps in early detection and personalized management of this aggressive disease. Drawing from cutting-edge research in molecular oncology, proteomics, and bioinformatics, this paper highlights key genetic drivers such as KRAS, TP53, CDKN2A, and SMAD4 mutations that fuel Pancreatic cancer progression and stromal desmoplasia. Diverse peptide sources, including tumor-derived neoantigens, stromal remodeling fragments, and immune-modulating signals and their release mechanisms via ectodomain shedding and exosomes, were explored. Emphasizing advanced discovery pipelines, from mass spectrometry-based proteomics to immunoassays and machine learning-driven validation, current work spotlights promising candidates like PF4, PRO-C11-511, and CXCL7, which enhance diagnostic accuracy (AUC up to 0.961) and predict outcomes when integrated with established markers like CA19-9. By overcoming limitations of current biomarkers, such as low specificity and stage-dependency. This review underscores peptides' role in revolutionizing precision oncology, paving the way for non-invasive screening, targeted therapies, and improved survival in pancreatic cancer patients.

The aggressive progression of head and neck cancer (HNC) and the limited availability of effective targeted therapies render it as a significant global health challenge. Several key biological pathways, including PI3K/AKT/mTOR, Wnt/β-catenin, AMPK, and glycolysis, play crucial roles in the progression of HNC. Although conventional therapies such as chemotherapy remain widely utilized, there is a pressing need for innovative interventions to address the major limitations of these approaches. In response to this critical issue, this study seeks to evaluate the efficacy of the FDA-approved drug metformin as an anti-cancer agent. To identify and assess the inhibition of these biological molecules by metformin analogs, we employed a comprehensive in-silico approach that integrated molecular docking, molecular dynamics (MD) simulations, and MM/PBSA (Molecular Mechanics/Generalized Born Surface Area) free energy calculations. PubChem compound CID 222300 emerged as a top-scoring ligand with a high binding affinity for the mTOR protein (PDB: 4JSV). A 100 ns MD simulation was conducted to evaluate the stability and conformational dynamics of the mTOR–ligand complex. The results demonstrated favourable interaction characteristics, including a consistently decreasing radius of gyration (Rg), low root mean square fluctuation (RMSF), and stable root mean square deviation (RMSD), indicating overall structural compaction and stability. Further evidence from hydrogen bond analysis revealed that the ligand contributed to complex stability by maintaining sporadic yet regular polar interactions throughout the trajectory. These findings suggest that CID 222300 is a promising lead compound capable of interacting with the mTOR target in a stable and targeted manner, indicating its potential as a novel therapeutic agent against HNC.